@techreport{oai:mie-u.repo.nii.ac.jp:00014493,
 author = {片山, 直之 and Katayama, Naoyuki},
 month = {May},
 note = {application/pdf, 免疫不全マウスへの異種移植系とin vitro培養系を用いて、CD25+急性骨髄性白血病においては白血病幹細胞分画のCD25の発現は変動することを明らかにし、CD25はCD25+急性骨髄性白血病の分子標的とはなり難いことが示した。成人B1細胞の起源を検討した。造血幹細胞に遺伝子異常を認めるが、その造血幹細胞が多分化能を保持している後天的疾患である発作性夜間血色素尿症と慢性骨髄性白血病の症例の末梢血液細胞を解析することで、成人造血幹細胞がB1細胞を産生していることを明らかにした。, We examined leukemic stem cell (LSC) properties of CD25-positive acute myeloid leukemia (AML), using a patient-derived xenograft model and an in vitro culture system. The expression of CD25 fluctuated in LSCs in CD25-positive AML, suggesting that targeting CD25 may not be effective for eradicating LSCs of CD25-positive AML.
We analyzed peripheral blood cells from patients with paroxysmal nocturnal hemoglobinemia (PNH), a clonal disorder of hematopoietic stem cells (HSCs) caused by somatic mutations in PIGA. Importantly, the PIGA-mutated HSCs retain their multilineage differentiation capacity. We separated and investigated the mutated cells. The results suggest that a small, but distinct, proportion of B1 cells may be derived from adult HSCs. The similar data were obtained with peripheral blood cells from patients with chronic myelogenous leukemia, a clonal disorder of HSCs with their multilineage differentiation capacity except for T-cell lineage., 2017年度～2019年度科学研究費補助金(基盤研究(C))研究成果報告書, 17K09923},
 title = {WT1を標的とした急性骨髄性白血病のキメラ抗原受容体発現T細胞療法の基盤構築},
 year = {2020},
 yomi = {カタヤマ, ナオユキ}
}